Seasonal Affective Disorder (SAD) is a clinically diagnosed syndrome that is hypothesized to represent the morbid extreme of a spectrum seasonality, a continuum that is assumed to span the general population in varying degrees of severity. Based on a self report survey carried out by investigators in our branch, an estimated 5% report a degree of change and impairment that resembles the response of patients clinically diagnosed with SAD. A high percentage of women make up that 5%, only 19% of individuals classified as having SAD are men. The more that we know about the nature of seasonality, the better we can determine whether it has an independent role in the development of differences in symptom presentation and treatment response that is found among depressed patients. The study is designed to test the following hypotheses using self report data from a population of clinically unselected twin pairs: (1) Genetic as well as environmental factors contribute to the etiology of seasonality. (2) There is a single dimension of vulnerability; the same genetic and environmental risk factors which determine risk of SAD also determine the differences in seasonality within the normal range. (3) Genetic vulnerability to seasonality is manifested by seasonal change in a broad spectrum of behaviors including sleep pattern, social activity, mood, weight, appetite and energy level. (4) There is a sex difference in the magnitude of the genetic contribution to risk of SAD. The sample for this study was drawn from an adult twin registry maintained by the Australian National Health and Medical Research Council. Included are a total of 2693 pairs that responded to a subsection of the Seasonal Pattern Assessment Questionnaire, a self-administered retrospective questionnaire designed to measure the presence, severity and pattern of seasonality. This instrument was included in a mailed questionnaire survey conducted by Martin and colleagues at the Queensland Institute of Medical Research. A series of genetic analyses were performed to study hypotheses. The results include: (1) There is a tendency for seasonality to run in families, and this is largely due to biological effects. Between 26-30% of the variance is determined by additive genetic effects, the remainder to environmental experiences unique to the individual (which do not contribute to family resemblance). (2) There is not one dimension of vulnerability, but two processes: one is a dichotomous process where separate genetic and environmental factors determine morbidity and normalcy; the second continuous in nature, with degrees of severity. (3) There does not appear to be a generalized genetic vulnerability to seasonal changes. Instead, distinct genetic factors are indicated to predispose to (i) weight and appetite changes; and (ii) mood and energy change. (4) As compared to males, females consistently have a greater proportion of their phenotypic variance accounted for by genetic effects. The findings support continuing efforts to determine the role of seasonality in the development of depressive disorder.